Ricerc@Sapienza

Lab webseite: https://sites.google.com/uniroma1.it/emculab-canettieri

Our laboratory is interested in understanding how epigenetic and metabolic reprogramming influence tumor behaviour and to invetigate the possibility to target these alterations for therapeutic purposes.

The current main topics of our lab are:

1) Energy and redox rewiring in Cancer

Altered metabolism is a hallmark of cancer, supporting uncontrolled proliferation and adaptation to stress. Our research focuses on how cancer cells reprogram energy production and redox homeostasis, particularly the balance between NADH and NAD⁺, to sustain growth. Changes in glycolysis, oxidative phosphorylation, and mitochondrial shuttles allow tumors to adapt their energy supply and maintain redox equilibrium under fluctuating nutrient conditions.

We are also interested in how redox alterations influence oncogenic signaling and the tumor microenvironment, and how these pathways can be targeted with pharmacological agents or dietary interventions. By studying the molecular basis of metabolic rewiring, we aim to uncover vulnerabilities in cancer metabolism that can be exploited for therapy. This line of research integrates cancer biology, metabolism, and translational approaches, with the long-term goal of developing strategies that selectively disrupt tumor energy and redox networks.

2) Targeting MYC biosynthesis and dowstream regulated pathways in Colorectal Cancer.

The MYC oncogene is aberanlty expressed in many forms of cancer, where it controls key tumorigetic steps, influencing the composition of the tumor microenvironment. Hence, its targeting is universally seen as a  valuable approach for cancer therapy. Our research focuses on how MYC is controlled at the level of protein synthesis.
We study how translation initiation (via mTOR/4EBP1) and elongation (via eIF5A hypusination) cooperate to sustain high MYC output.
This connects metabolic pathways, such as polyamine biosynthesis, directly to oncogene expression.
We are interested in how these mechanisms shape the tumor microenvironment and influence therapy response.
Our approach combines molecular biology, metabolism, and cancer models to map these regulatory circuits.
We test pharmacological and genetic interventions that target polyamine metabolism, eIF5A hypusination, and mTOR signaling.
We explore combination therapies that collapse compensatory translation programs.
The goal is to identify therapeutically actionable vulnerabilities in MYC-driven CRC.
In the short term, we develop biomarkers of translational dependency. In the long term, we aim to translate these findings into novel treatment strategies for patients

3) Role of microbiota in regulating cancer initiation and progression via epigenetic mechanisms 

Emerging evidence show that microorganisms play a key role during tumorigenesis by altering tumor microenvironment and affecting specific oncogenic patways. We are characterizing signaling molucules, metabolites and specific pathways connecting microbiota sensing to epigenetic remodeling in cancer stem cells and the immune system.